The myometrium, which is the smooth muscle component of the uterus, undergoes hypertrophy as parturition (birth) approaches. Hormones play an important role in this response. The smooth muscle is quiescent during pregnancy when the hormone progesterone predominates, and few gap junctions that electrically couple the smooth muscle cells are present. At term, under the dominant influence of estrogen, the myometrium undergoes marked hypertrophy. Large numbers of gap junctions form just before birth and convert the myometrium to a single-unit tissue to coordinate contraction during parturition.
The growth and development of tissues that contain smooth muscle are associated with increases in the connective tissue 1.4 1.2 1.0 0.8 0.6 0.0 •Fig. 14.14 Smoothmusclecellscarryoutmanyactivities.A,Theyretainthecapacitytodivideduringnormalgrowthorincertainpatho logicalresponsessuchasformationofatheroscleroticplaque.B,Cellsmayalsohypertrophyinresponsetoincreasedloads.Chromosomalreplicationnotfollowedbycelldivisionyieldscellswithagreatercontentofcontractileproteins.C,Smoothmusclecellsalsosynthesizeandsecretetheconstituentsoftheextracellularmatrix.
Althoughsmoothmuscleisinvolvedinphysiologicaladjustmentstoexercise,sustainedchangesinthe mechanicalloadingthatinducecellularadaptationsareusuallytheresultofapathologicalcondition(e.g.,hypertension).Afairlycommonexampleinmenisurinary bladder hypertrophy causedbybenignorcancerous enlargementoftheprostategland,whichobstructsthebladderoutlet.Theclinicalresultisdifficultyurinating, •Fig. 14.13 Myogenicresponseinvascularsmoothmuscleisanautoregulatoryresponsetomaintainconstantflowtoatissue.Anincreaseintransmuralpressure(TMP; top panel) elevatesintracellular[Ca++](middle panel), resultinginavasoconstriction(bottom panel). Notethattheincreaseintransmuralpressureinitiallystretchestheskeletalmuscleresistanceartery(bottom panel), butthisisquicklyfollowedbyvasoconstriction.(FromSchubertRetal.Cardiovasc Res 2008;77:8-18.) matrix. Smooth muscle cells can synthesize and secrete the materials that make up this matrix, including collagen, elastin, and proteoglycans (see
Fig. 14.14 ). The synthetic and secretory capacities are evident when smooth muscle cells are isolated and placed in tissue culture. The cells rapidly distentionofthebladder,andimpairedemptying.Inthissituationtheabilityofthebladdersmoothmuscletocontractanddevelopstressisdiminished.Thereasonsforthisremainunexplained,butphenotypicmodulationofthesmoothmusclecellswithalteredcontractileproteinisoformexpressionandgrossanatomicdistortionofthebladderwalloccurs.NeuromuscularchangesalsoaffectmyoplasmicCa++ mobilizationandcross-bridgephosphorylation.Fortunately,normalstructureandfunctionareusuallyrestoredaftertheobstructionisalleviated.
lose thick myosin filaments and much of the thin-filament lattice, and there is expansion of the rough endoplasmic reticulum and Golgi apparatus. The phenotypically altered cells multiply and lay down connective tissue. This process is reversible, and some degree of redifferentiation with the formation of thick filaments occurs after cell replication ceases. Determinants of the smooth muscle cell phenotype are largely unknown, but hormones and growth factors in blood, as well as mechanical loads on cells, have been implicated in the control of phenotypic modulation.